The invention disclosed herein is a cardiac pacemaker that responds to varying physiological or metabolic requirements of the body by automatically adjusting the stimulus or pacing rate and, hence, the blood pumping rate of an abnormal heart to the same extent that the body would naturally adjust the rate of a normal heart for equivalent physiological requirements.
The body maintains a hormone level in the blood that is related to the prevailing amount of physical activity and emotional stress. When a person increases physical activity voluntarily or is subjected to a challenge that results in stress, the level of the activating hormones increases. By a complex but short duration chain of events, the heart responds to the hormone level or direct nerve action by beating at a higher rate so as to pump a sufficient volume of blood for coping with the increased demand. The converse of the foregoing occurs when the person goes from a physically active state to a resting state.
Normally, changes in physical activity alter the rate of the nerve impulses to the sino-atrial (SA) node of the heart. This node depolarizes in response to receiving said nerve impulses and causes an electric signal to be propagated over the atrium which causes it to contract and discharge blood into the ventricles. The atrial signal is conducted to the atrio-ventricular (AV) node which, after a short delay, causes a depolarizing signal to be propagated over the ventricles, thus causing the ventricles to contract and to discharge blood to the aorta and pulmonary artery. Simultaneously with increased rate, ventricular contractility is enhanced.
The electrical system of the heart is subject to various kinds of failures. In some cases, the natural or intrinsic electric signals of the atrium occur at a rate in correspondence with hormone levels and physiological requirements but the signals are not propagated to or through the Purkinje fibers which conduct the signals from the AV node to the ventricles. Hence, the ventricles do not depolarize immediately in which case ventricular contraction is delayed and falls out of synchronism with the atrium. The ventricles have an escape capability which is to say that even though they do not receive a conducted signal they will depolarize by themselves eventually and cause ventricular contraction. This slow ventricular rate results in an inadequate supply of blood to the organs which reduces patient's work capacity and can result in a patient fainting, especially if an attempt is made to increase activity.
In some individuals, the defect in the electrical system of the heart is such that the heart generates natural or intrinsic stimulus signals some of the time but fails to generate them at other times. Pacemakers that provide artificial electric stimuli on demand are usually implanted in the subject when ventricular contractions are missed or unduly delayed periodically. The latest demand pacemaker designs can be programmed from outside of the body to operate in any of several modes. For instance, a pacemaker may be controlled to pace the atrium only, or to pace ventricles only, or to pace the heart chambers synchronously, first the atrium, then delay, then ventricle stimulation. In demand pacemakers, the pacing rate is set sufficiently high to assure that enough blood will be pumped to permit a limited amount of physical activity above a resting state.
In some cases the pacemaker is operated in the atrial synchronous mode. The atrial signal is detected and used to adjust the artificial stimulus or pacing rate of the pacing pulse generator in the ventricle to match physiological requirements. This is based on the assumption that the nerve impulses to the SA node increase and decrease faithfully in response to changes in demand. There is coordination between the natural atrial signal timing and variable physiological requirements, but the signals are difficult to detect with accuracy. In some subjects, the atrial signal is not synchronized with the ventricular signal. U.S. Pat. No. 4,313,442 exhibits one attempt to solve this problem.
It is known that with a healthy heart, the QT interval in the natural ECG signal changes in relation to physiological demand, that is, the QT interval shortens as exercise is increased. U.S Pat. No. 4,228,803 uses this phenomenon to adjust the artificial stimulus pulse rate in relation to physiological requirements. The interval between the QRS complex in the ECG waveform and the T-wave is measured for every heart beat. As the T-wave interval shortens, the rate of the stimulus pulse generator is increased and as the interval lengthens, the pulse rate is decreased. This has not completely solved the problem of coordinating pacing rate with physiological demand because the QT interval is not wholly independent of pacing rate. When physical activity of the person is increased voluntarily, a natural contribution to shortening the T-wave interval occurs. The pacemaker senses this as a requirement for increasing the artificial stimulus rate. This shortens the interval further. Thus, there is a positive feedback and the pacemaker can go into a needless cycle of self-acceleration. Pacemakers of this type can increase the stimulus pulse rate even though physical activity has not increased.
Other attempts have been made to match stimulus pulse rate with physiological needs. One example is given in U.S. Pat. No. 4,009,721 which is based on recognition that the pH level of the blood is a function of physical activity. The pH is detected and converted to a signal useful for adjusting the rate of the stimulus pulse generator. However, there is doubt as to whether a system can respond to physiological requirements on a beat-to-beat basis.
A deficiency that exists in all prior art pacemakers which attempt to respond to physiological requirements is that they do not change stimulus rate in response to emotional stress or simply a challenge to the body without increase in physical activity as nature provides in a healthy individual with a normal heart.